APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy

摘要: Apolipoprotein L1 (APOL1) genetic variants are potent risk factors for glomerular disease, but one or more additional required expression of disease. Uncontrolled poorly controlled human immunodeficiency virus (HIV) infection is the most susceptibility factor APOL1 nephropathy that has been identified to date. associated with HIV-associated (HIVAN), a podocyte not HIV-immune complex primarily disease mesangium. The mechanism by which HIV brings out latent remains be defined. There at least two classes candidate mechanisms explain interaction between HIV-1 and APOL1. First, variant proteins accessory implicated in HIVAN may target same related intracellular pathways podocytes. Recent data suggest roles interleukin 1b transcription EB. Second, features uncontrolled infection, including increased circulating such as interferon, drive gene act upon podocytes other ways. Deeper probing APOL1-HIV interactions yield insights will aid understanding HIVAN, nephropathy, biology.